Difference between revisions of "Amniotic fluid embolism"
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== Risk Factors<!-- List and briefly describe any procedures which may be performed specifically to treat this comorbidity or its sequelae. If none, this section may be removed. -->== | == Risk Factors<!-- List and briefly describe any procedures which may be performed specifically to treat this comorbidity or its sequelae. If none, this section may be removed. -->== | ||
Risk factors for the development of AFE are advanced maternal age, multiparity, male fetuses, and trauma. | Risk factors for the development of AFE are advanced maternal age, multiparity, male fetuses, and trauma. Induction of labor has also been found to increase risk for AFE. | ||
== Pathophysiology<!-- Describe the pathophysiology of this comorbidity. Add subsections as needed. --> == | == Pathophysiology<!-- Describe the pathophysiology of this comorbidity. Add subsections as needed. --> == | ||
AFE is poorly understood. | AFE is poorly understood. It is thought to originate from a disruption of the placenta-amniotic interface with the subsequent entry of amniotic fluid and fetal elements (such as hair, meconium, squama, and mucin) into the maternal circulation. Upon entering the pulmonary tree, intense pulmonary vasoconstriction occurs. This may be associated with concomitant bronchoconstriction. The hemodynamic result is acute pulmonary arterial obstruction, dilatation of the right ventricle and the right atrium, and significant tricuspid regurgitation. The right ventricular enlargement causes the intraventricular septum to bow into the left ventricle creating obstruction and systolic dysfunction, further raising pulmonary artery pressure and decreasing cardiac output. Hypoxemia and hypotension lead to sudden cardiovascular collapse. | ||
Normally, pregnancies are procoagulant, to begin with, and the introduction of amniotic fluid and fetal elements trigger inflammatory mediators activating the coagulation cascade and fibrinolytic systems resulting in DIC. | |||
== Signs and symptoms<!-- Describe the signs and symptoms of this comorbidity. --> == | == Signs and symptoms<!-- Describe the signs and symptoms of this comorbidity. --> == | ||
== Diagnosis<!-- Describe how this comorbidity is diagnosed. --> == | == Diagnosis<!-- Describe how this comorbidity is diagnosed. --> == | ||
The American Society for Maternal-Fetal Medicine, after a consensus symposium has created its criteria for AFE, which require the following: | |||
# Sudden cardiopulmonary collapse, or hypotension (systolic blood pressure less than 90 mmHg) with hypoxia (SpO2 less than 90%) | |||
# DIC, according to the international society on thrombosis and hemostasis (ISTH) definition | |||
# Symptomatology either during labor or during placental delivery (or up to 30 minutes later) | |||
# No fever | |||
== Treatment<!-- Summarize the treatment of this comorbidity. Add subsections as needed. --> == | == Treatment<!-- Summarize the treatment of this comorbidity. Add subsections as needed. --> == | ||
Revision as of 12:47, 20 October 2022
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An amniotic fluid embolism (AFE) is a rare but serious condition with high morbidity and mortality. It is characterized by cardiopulmonary collapse and disseminated intravascular coagulation (DIC). It is the second-leading cause of peripartum maternal death in the US and number one cause of peripartum cardiac arrest. [1]
Anesthetic implications
Preoperative optimization
Intraoperative management
Postoperative management
Risk Factors
Risk factors for the development of AFE are advanced maternal age, multiparity, male fetuses, and trauma. Induction of labor has also been found to increase risk for AFE.
Pathophysiology
AFE is poorly understood. It is thought to originate from a disruption of the placenta-amniotic interface with the subsequent entry of amniotic fluid and fetal elements (such as hair, meconium, squama, and mucin) into the maternal circulation. Upon entering the pulmonary tree, intense pulmonary vasoconstriction occurs. This may be associated with concomitant bronchoconstriction. The hemodynamic result is acute pulmonary arterial obstruction, dilatation of the right ventricle and the right atrium, and significant tricuspid regurgitation. The right ventricular enlargement causes the intraventricular septum to bow into the left ventricle creating obstruction and systolic dysfunction, further raising pulmonary artery pressure and decreasing cardiac output. Hypoxemia and hypotension lead to sudden cardiovascular collapse.
Normally, pregnancies are procoagulant, to begin with, and the introduction of amniotic fluid and fetal elements trigger inflammatory mediators activating the coagulation cascade and fibrinolytic systems resulting in DIC.
Signs and symptoms
Diagnosis
The American Society for Maternal-Fetal Medicine, after a consensus symposium has created its criteria for AFE, which require the following:
- Sudden cardiopulmonary collapse, or hypotension (systolic blood pressure less than 90 mmHg) with hypoxia (SpO2 less than 90%)
- DIC, according to the international society on thrombosis and hemostasis (ISTH) definition
- Symptomatology either during labor or during placental delivery (or up to 30 minutes later)
- No fever
Treatment
Medication
Surgery
Prognosis
Epidemiology
References
- ↑ Haftel, Anthony; Chowdhury, Yuvraj S. (2022), "Amniotic Fluid Embolism", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 32644533, retrieved 2022-10-20